Evidence map›Paper›PMID 18347325›Full record

ArticleGenome research2008

Using ChIP-chip technology to reveal common principles of transcriptional repression in normal and cancer cells.

Vitalina M Komashko, Luis G Acevedo, Sharon L Squazzo, Sushma S Iyengar, Alina Rabinovich, Henriette O'Geen, Roland Green, Peggy J Farnham

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Genome research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  4. Axitinib blocks Wnt/β-catenin signaling and directs asymmetric cell division in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  5. HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
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  19. Open chromatin in pluripotency and reprogramming.Nature reviews. Molecular cell biology · 2011
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Vitalina M KomashkoDepartment of Pharmacology and the Genome Center, University of California-Davis, Davis, California 95616, USA.
Luis G Acevedo
Sharon L Squazzo
Sushma S Iyengar
Alina Rabinovich
Henriette O'Geen
Roland Green
Peggy J Farnham
University of California, Davis · US

Funding

Discovery of Binding Sites for Transcription FactorsR01HG003129 · NHGRI · NIMBLEGEN SYSTEMS, INC. · PI GREEN, ROLAND D · 2003 to 2006
$1.6M
Mechanisms of Transcriptional Regulation in Stem CellsR01DK067889 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI FARNHAM, PEGGY J · 2005 to 2007
$649k
Mechanisms of Transcriptional Regulation in Stem CellsR56DK067889 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FARNHAM, PEGGY J · 2009 to 2009
$222k
NCI NIH HHS CA45250NHGRI NIH HHS HG003129NHGRI NIH HHS R01 HG003129NIDDK NIH HHS DK067889NIDDK NIH HHS R01 DK067889NIDDK NIH HHS R56 DK067889
6 · The paper itself

Abstract

We compared 12 different cell populations, including embryonic stem cells before and during differentiation into embryoid bodies as well as various types of normal and tumor cells to determine if pluripotent versus differentiated cell types use different mechanisms to establish their transcriptome. We first identified genes that were not expressed in the 12 different cell populations and then determined which of them were regulated by histone methylation, DNA methylation, at the step of productive elongation, or by the inability to establish a preinitiation complex. For these experiments, we performed chromatin immunoprecipitation using antibodies to H3me3K27, H3me3K9, 5-methyl-cytosine, and POLR2A. We found that (1) the percentage of low expressed genes bound by POLR2A, H3me3K27, H3me3K9, or 5-methyl-cytosine is similar in all 12 cell types, regardless of differentiation or neoplastic state; (2) a gene is generally repressed by only one mechanism; and (3) distinct classes of genes are repressed by certain mechanisms. We further characterized two transitioning cell populations, 3T3 cells progressing from G0/G1 into S phase and mES cells differentiating into embryoid bodies. We found that the transient regulation through the cell cycle was achieved predominantly by changes in the recruitment of the general transcriptional machinery or by post-POLR2A recruitment mechanisms. In contrast, changes in chromatin silencing were critical for the permanent changes in gene expression in cells undergoing differentiation.

Indexed as

Gene Expression Regulation, NeoplasticGene SilencingAnimalsCell DifferentiationCells, CulturedChromatin ImmunoprecipitationCluster AnalysisDNA MethylationEmbryonic Stem CellsGene Expression ProfilingHistonesHumansMiceNIH 3T3 CellsOligonucleotide Array Sequence AnalysisPromoter Regions, GeneticHistones

Identifiers

PMID18347325
PMCPMC2279240
OpenAlexW2105123252

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.